[250mg tablet 7 cents]
- Lithicarb, lithium carbonate, priadel
- treatment of bipolar disorder
PRESENTATION AND ADMINISTRATION:
Lithicarb FC 250mg and 400mg tablets (white)
Lithium carbonate capsules 250mg (green / clear)
Controlled Release Tablets:
400mg tablets (white)
Usual maintenance dosage 250mg – 1200mg daily in divided doses twice a day for tablets and capsules and daily for controlled release tablets (adjusted to levels)
Note: no information is available on NG administration; check with pharmacist if necessary
DOSAGE IN RENAL FAILURE AND RENAL REPLACEMENT THERAPY:
- Avoid is possible if GFR <50. If lithium must be used, reduce levels and monitor plasma concentration carefully
DOSAGE IN PAEDIATRICS:
5-20mg/kg 8-24 hourly; do not use controlled release tablets
- Lithium is an element of the alkali-metal group. Preclinical studies have shown that lithium alters sodium transport in nerve and muscle cells and effects a shift toward intraneuronal metabolism of catecholamines, but the specific biochemical mechanism of lithium action in mania is unknown.
- significant renal or cardiovascular disease
- severe dehydration
- sodium depletion
- patients receiving diuretics
- Lithium Toxicity
The likelihood of toxicity increases with increasing serum lithium levels. Serum lithium levels greater than 1.5 mEq/l carry a greater risk than lower levels. However, patients sensitive to lithium may exhibit toxic signs at serum levels below 1.5 mEq/l. Diarrhoea, vomiting, drowsiness, muscular weakness and lack of coordination may be early signs of lithium toxicity, and can occur at lithium levels below 2.0 mEq/l. At higher levels, giddiness, ataxia, blurred vision, tinnitus and a large output of dilute urine may be seen. Serum lithium levels above 3.0 mEq/l may produce a complex clinical picture involving multiple organs and organ systems. Serum lithium levels should not be permitted to exceed 2.0 mEq/l during the acute treatment phase.
- Nephrogenic diabetes insipidus
Chronic lithium therapy may be associated with diminution of renal concentrating ability, occasionally presenting as nephrogenic diabetes insipidus, with polyuria and polydipsia. Such patients should be carefully managed to avoid dehydration with resulting lithium retention and toxicity. This condition is usually reversible when lithium is discontinued.
Lithium decreases sodium reabsorption by the renal tubules which could lead to sodium depletion. In addition to sweating and diarrhoea, concomitant infection with elevated temperatures may also necessitate a temporary reduction or cessation of medication.
- Laboratory Tests:
Lithium levels should be checked in any patient on lithium admitted to the Intensive Care Unit. Samples should be collected in a yellow top tube (SST) and should be taken 12 hours post-dose. The therapeutic range is 0.6-1.2mmol/L In the setting of acute overdose, peak levels of >5mmol/L 4-8 hours after ingestion are not unusual.
- Drug/Laboratory Test Interactions:
IMPORTANT DRUG INTERACTIONS FOR THE ICU
- Combined use of Haloperidol and Lithium An encephalopathic syndrome (characterized by weakness, lethargy, fever, tremulousness and confusion, extrapyramidal symptoms, leucocytosis, elevated serum enzymes, BUN and FBS) followed by irreversible brain damage has occurred in a few patients treated with lithium plus haloperidol. A causal relationship between these events and the concomitant administration of lithium and haloperidol has not been established; however, patients receiving such combined therapy should be monitored closely for early evidence of neurological toxicity and treatment discontinued promptly if such signs appear. Lithium may prolong the effects of neuromuscular blocking agents. Therefore, neuromuscular blocking agents should be given with caution to patients receiving lithium. Caution should be used when lithium and diuretics or angiotensin converting enzyme (ACE) inhibitors are used concomitantly because sodium loss may reduce the renal clearance of lithium and increase serum lithium levels with risk of lithium toxicity. Lithium levels should be closely monitored when patients initiate or discontinue NSAID use. In some cases, lithium toxicity has resulted from interactions between an NSAID and lithium.
Tremor, muscle hyperirritability (fasciculations, twitching, clonic movements of whole limbs), ataxia, choreo-athetotic movements, hyperactive deep tendon reflexes. Central Nervous System: Blackout spells, epileptiform seizures, slurred speech, dizziness, vertigo, incontinence of urine or feces, somnolence, psychomotor retardation, restlessness, confusion, stupor, coma, acute dystonia, downbeat nystagmus.
Cardiac arrhythmia, hypotension, peripheral circulatory collapse, sinus node dysfunction with severe bradycardia (which may result in syncope).
Cases of pseudotumor cerebri (increased intracranial pressure and papilledema) have been reported with lithium use.
Anorexia, nausea, vomiting, diarrhea.
Albuminuria, oliguria, polyuria, glycosuria.
Drying and thinning of hair, anesthesia of skin, chronic folliculitis, xerosis cutis, alopecia and exacerbation of psoriasis.